Headrick J P, Angello D A, Berne R M
Department of Physiology, University of Virginia, Charlottesville 22908.
Circulation. 1990 Dec;82(6):2163-9. doi: 10.1161/01.cir.82.6.2163.
The loss of coronary vasodilator reserve after ischemia-reperfusion may be due to endothelial injury, and this vascular dysfunction may contribute to functional alterations observed after ischemia. To determine whether endothelial dysfunction occurs after relatively brief periods of moderate low-flow ischemia in vivo, open-chest swine were subjected to 15 minutes of critical, subtotal left anterior descending coronary artery occlusion (80%) followed by 60 minutes of reperfusion. Serial measurements of regional coronary flow were made with the radiolabeled microsphere technique. After 60 minutes of reperfusion, the left anterior descending coronary artery was excised together with a section of the normally perfused left circumflex coronary artery to examine in vitro the relaxations to the endothelium-dependent dilators ADP and bradykinin and to the endothelial-independent dilators sodium nitroprusside and adenosine. Contractions to serotonin in quiescent rings were also examined. Endocardial and transmural blood flows recovered to preocclusion levels within 60 minutes of reperfusion, as did the epicardial-to-endocardial ratio. Vascular responses in isolated, reperfused left anterior descending coronary artery rings were significantly different from responses in control left circumflex coronary artery rings. Endothelium-dependent relaxations to adenosine diphosphate and bradykinin were significantly depressed in the left anterior descending coronary artery rings compared with left circumflex coronary artery rings (p less than 0.05). Serotonin-induced contractions were significantly greater in occluded-reperfused left anterior descending than in left circumflex coronary arteries (p less than 0.05). Relaxations to adenosine and sodium nitroprusside were not significantly different between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
缺血再灌注后冠状血管扩张储备的丧失可能是由于内皮损伤,这种血管功能障碍可能导致缺血后观察到的功能改变。为了确定在体内相对短暂的中度低流量缺血后是否会发生内皮功能障碍,对开胸猪进行了15分钟的临界、左前降支冠状动脉次全闭塞(80%),随后再灌注60分钟。用放射性标记微球技术对局部冠状动脉血流进行连续测量。再灌注60分钟后,切除左前降支冠状动脉及其一段正常灌注的左旋支冠状动脉,以体外检测对内皮依赖性扩张剂ADP和缓激肽以及对内皮非依赖性扩张剂硝普钠和腺苷的舒张反应。还检测了静息环中对5-羟色胺的收缩反应。再灌注60分钟内心内膜和透壁血流恢复到闭塞前水平,心外膜与心内膜比值也恢复到闭塞前水平。离体再灌注的左前降支冠状动脉环的血管反应与对照左旋支冠状动脉环的反应显著不同。与左旋支冠状动脉环相比,左前降支冠状动脉环对二磷酸腺苷和缓激肽的内皮依赖性舒张反应明显降低(p<0.05)。闭塞再灌注的左前降支冠状动脉中5-羟色胺诱导的收缩明显大于左旋支冠状动脉(p<0.05)。两组对腺苷和硝普钠的舒张反应无显著差异。(摘要截短于250字)